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Obesity is heterogeneous, and visceral adipose tissue (VAT) dysfunction (\u2018adiposopathy\u2019) complicates risk stratification. Osteopontin (OPN) is a pleiotropic mediator implicated in VAT inflammation, senescence\u2010associated pathways, atherosclerosis and myocardial remodelling.<\/jats:p>\n                  <\/jats:sec>\n                  <jats:sec>\n                    <jats:title>Methods<\/jats:title>\n                    <jats:p>We performed a narrative synthesis of preclinical and clinical evidence on OPN across three domains: (i) VAT biology and senescence\u2010associated secretory phenotype (SASP); (ii) atherosclerosis and plaque vulnerability; and (iii) myocardial fibrosis\/remodelling and cardiometabolic heart failure. We also summarize biomarker and therapeutic implications.<\/jats:p>\n                  <\/jats:sec>\n                  <jats:sec>\n                    <jats:title>Results<\/jats:title>\n                    <jats:p>OPN is increased in obesity, particularly within VAT, where it contributes to SASP\u2010related signalling, macrophage dysfunction, low\u2010grade systemic inflammation, insulin resistance and cardiometabolic risk. Clinical and translational studies link circulating and tissue OPN levels to vascular inflammation, plaque vulnerability and adverse CV events. In the myocardium, OPN appears to act as a remodelling\u2010specific mediator connecting extracardiac adiposity\u2010related signals to interstitial fibrosis, with the strongest evidence in heart failure with preserved ejection fraction and diabetic cardiomyopathy. Across settings, OPN shows promise as an early biomarker for detection and risk stratification. Experimental modulation of OPN attenuates fibrosis and improves cardiac function in multiple models, supporting its candidacy as a mechanistic therapeutic target.<\/jats:p>\n                  <\/jats:sec>\n                  <jats:sec>\n                    <jats:title>Conclusions<\/jats:title>\n                    <jats:p>OPN likely bridges the fat\u2013heart axis through senescence\u2010related pathways and may help explain residual CV risk in obesity\u2010related cardiometabolic disease. Standardized assays, prospective validation and interventional studies are required to establish clinical utility for OPN as a biomarker and therapeutic target.<\/jats:p>\n                  <\/jats:sec>","DOI":"10.1111\/eci.70181","type":"journal-article","created":{"date-parts":[[2026,1,21]],"date-time":"2026-01-21T12:03:39Z","timestamp":1768997019000},"update-policy":"https:\/\/doi.org\/10.1002\/crossmark_policy","source":"Crossref","is-referenced-by-count":2,"title":["The fat\u2010heart entanglement and the role of \u2018osteopontin mechanics\u2019 in cardiometabolic senescence"],"prefix":"10.1111","volume":"56","author":[{"given":"Cristina","family":"Michelauz","sequence":"first","affiliation":[{"name":"First Clinic of Internal Medicine, Department of Internal Medicine University of Genoa  Genoa 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